Signal transduction for IL-17A and IL-17F, mainly produced by activated TH17 cells, requires the presence of a heterodimeric complex consisting of the ubiquitously expressed IL-17RA and the inducible IL-17RC, and the absence of either receptor results in ineffective signaling.29 Thus, our data implicates an impaired mucosal IL-17A/F signaling in IBD, known to be important for host response and clearance of extracellular pathogens,30 irrespective of disease activity. This evidence concerns the gene IL17A and inflammatory bowel disease.